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Author
Topic: New Mutation!! (Read 10675 times)

Well, I just got my latest genotype back...and come to find out my little HIV darlings have mutated and I am now resistant to Combivir! I have to make yet another med switch, this makes two in one month! Yuck! Oh well...we will see...

Sorry to hear about this bud. Two med switches in a month, that's rough. Are you resistant to both AZT as well as 3TC? I'm pretty sure you'll get expert suggestions from people here. And you seem to have an amazing pragmatic attitude, which rawks. (I learn new words from Ameds every day )

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Her finely-touched spirit had still its fine issues, though they were not widely visible. Her full nature, like that river of which Cyrus broke the strength, spent itself in channels which had no great name on the earth. But the effect of her being on those around her was incalculably diffusive: for the growing good of the world is partly dependent on unhistoric acts; and that things are not so ill with you and me as they might have been, is half owing to the number who lived faithfully a hidden life, and rest in unvisited tombs.

Check with your doctor if it's time to begin with Fuzeon. It has been the only med to get me undetectable in 20 years and I am also resistant to everything else till last year. Let's see if 2007 brings the new meds people are talking about. I'm sending you a private email now so check it out later...

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Catman

Meow to the birdsMeow to the tree'sMeow to the endof this dreadful disease...

Regarding the genotype tests, coincidentally I just read over at the research forum that there is a report of a new hiv test with " a level of sensitivity that makes the assay about 1,000 times more sensitive than the most widely used assays on the market for detecting drug-resistant HIV viruses".

Jeromy, I am sorry to here this but hopeful your doctor finds the puzzle fix... Jeromy did you have a resistant virus to begin with? I was under the impression you have been on meds for not a very long time..

Hey Jeromy, sorry like everyone else to hear about your resistance problem. One good thought which came to me is that given the two drugs involved, it may be how old and so passed around they are, rather than your virus somehow cleverly working around a brand new one/type. With fingers crossed for a quick resolution, Win

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Winthrop Smith has published three collections of poetry: Ghetto: From The First Five; The Weigh-In: Collected Poems; Skin Check: New York Poems. The last was published in December 2006. He has a work-in-progress underway titled Starting Positions.

Jeromy....There is a great light that shines from you....your smile is more infectious than any disease known to man! So with these powers of light this moment of darkness will not last! Remember that the sun shines every day....although the clouds would have us believe otherwise! Do not put power in the clouds my friend for your LIGHT will prevail!!

Jeromy-Like the posting prior to mine said that ur smile is infectious.

Sorry to hear about ur mutation. Unfortunately I am not sure how that is cuz I have been on the same combo for over a yr, but I think I understand how stressful it can b for changing meds that often. To my understanding, each med(s) have different side-effects. Changing between ediff meds in a given month must have given ur share of side effects. I again have never been on either, so forgive me for my lack of knowledge on either of the meds.

I just hope that ur doc has some suggestions of which med to take. Best of luck!

Sorry to hear whats happenning. But see if you can get a copy of that report, and perhaps post some of the information. You may get some ideas or suggestions.

Ray

I have attached a copy of the report here...I am resistent to the following:

EmtrivaEpivir

With a reduced susceptibility to Zerit, Retrovir, and Viread.

I also now have Dual-Tropic HIV or Mixed Population...I have both CCR5 and CXCR5 tropisms. This is from being on the Marviroc study: the CCR5 entry inhibitor. What seems to have happened, at the beginning of the study I was only CCR5, and I have now changed tropisms...so, I am no longer able to take a CCR5 inbitor (fusion or entry). Meaning that Fuzeon is no longer an option for me.

So...I will chat with the doctor this afternoon and see what the options are going to be...

Well...doctor called and because of my latest results where my CD4 counts are good and my VL is undetectible, we have decided to keep my regimen for now. It seems to working...so we will keep an eye on things over the next couple of months and get a better guage in March.

Here is a little bit of the article on aidsmeds that might explain why stay with Epivir still helps:

However, Epivir resistance might make the virus even more sensitive to other NRTIs, most notably Retrovir (even if HIV has mutations in its structure that would normally cause it to be resistant to Retrovir) and Viread.

Fuzeon is neither CCR5 nor CXCR4 tropism dependant. It binds to neither receptor. Fuzeon (ENF) binds to the first heptad-repeat (HR1) in the GP41 subunit of the viral envelope glycoprotein, thus preventing conformational changes required for fusion of the viral envelope and CD4 cell membrane. It's mechanism of action is independent of the tropism . The prescribing information indicates ENF is equally active in vitro against clades A, AE, C, D, E, F, and G as well as R5, X4, and dual-tropic viruses.

I don't see ENF on either of the genotype reports you listed, and I'm far too lazy to look up what mutations are resistant to ENF. Anyways, it may still be an option for you in the future..

It is a moot point since you are currently going to stay the course with your current regimen (which to me seems like a good call, if it ain't broke, don't fix it).

As a matter of curiosity, how can they get an accurate genotype if your VL is undetectable (I'm assuming you mean less than 50)? I wasn't aware it could be done.

Resistance testing may be useful for some with 'undetectable' viral loads

Genotypic resistance testing in individuals with an 'undetectable' viral load may be more reliable than currently thought, according to a report published in the September issue of the Journal of Acquired Immune Deficiency Syndromes. They argue that resistance testing in those with very low detectable HIV RNA levels (e.g. between four and 75 copies/ml) may be useful to inform treatment decisions in individuals who are experiencing viral load 'blips' or an unexpectedly slow response to a change in their antiretroviral regimen.

Fuzeon is neither CCR5 nor CXCR4 tropism dependant. It binds to neither receptor. Fuzeon (ENF) binds to the first heptad-repeat (HR1) in the GP41 subunit of the viral envelope glycoprotein, thus preventing conformational changes required for fusion of the viral envelope and CD4 cell membrane. It's mechanism of action is independent of the tropism . The prescribing information indicates ENF is equally active in vitro against clades A, AE, C, D, E, F, and G as well as R5, X4, and dual-tropic viruses.

I don't see ENF on either of the genotype reports you listed, and I'm far too lazy to look up what mutations are resistant to ENF. Anyways, it may still be an option for you in the future..

It is a moot point since you are currently going to stay the course with your current regimen (which to me seems like a good call, if it ain't broke, don't fix it).

As a matter of curiosity, how can they get an accurate genotype if your VL is undetectable (I'm assuming you mean less than 50)? I wasn't aware it could be done.

-Whizzer

Well, the genotype was collected on Nove 16, and it took 6 weeks to get the results back. It was during that time that we switched from the Maraviroc to the Kaletra and remained on the Combivir. I wasn't undetectable then...My VL was aprroaching a little over 1000, so there was enough there to collect the data.

Now, my VL is <75 which was they are considering to be undectible...so, with the way my numbers are now, we aren't going to worry too much about the mutations until we see numbers slipping...

And thank you SO much for the info on Fuzeon, apparently I was misinformed...phew! But I can tell you I am no longer able to take the CCR5 entry inhibitors now...

Well...doctor called and because of my latest results where my CD4 counts are good and my VL is undetectable, we have decided to keep my regimen for now. It seems to working...so we will keep an eye on things over the next couple of months and get a better gauge in March.

So...wait and see as they say...

I was thinking the same way since your current cocktail is controlling your virus I wouldn't be so quick to change. My original doctor changed my meds so often trying to get me undetectable that my genotype had me resident to most of the meds a year ago when I got the PML so my doctor put me on Trizivir which the report showed some Resistance but here I am undetectable. We'll all be here with you waiting until March.Hugs

I wanted to pose what might be viewed as a bit of a sensitive question here, but I hope you'll appreciate me raising it both out of concern for you personally and to discuss the question in the broader sense once again:

Is your doctor aware at all of your current porn work?

Do you think that there might be a potential for setting yourself up for mutation problems through the type of sex activity involved with that particular style of porn work? I know the data behind the concepts of ''reinfection'' and/or ''superinfection'' are up for debate, but I was wanting get some current word from anyone more in the know than myself about what the latest word on this topic was. It just crossed my mind that if there was a lot of fluid exchange between yourself and someone else who was already Combivir resistant, wouldn't that expedite resistance in you? If so, might that problem potentially repeat itself?

"It just crossed my mind that if there was a lot of fluid exchange between yourself and someone else who was already Combivir resistant, wouldn't that expedite resistance in you? "

Theoretically, yes. But (1) the source would have to have enough virus to transmit - if he was undetectable this would be unlikely ... (2) the host would have to be immunologically receptive - who knows?

The most likely explanation for J's mutations, which don't seem that important anyway, is that he was on a combo that didn't get his viral load undetectable.